Genome-wide CRISPR Screens Reveal Host Factors Critical for SARS-CoV-2 Infection

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表观遗传学研究进展

表观遗传学是在基因组DNA序列不发生变化的条件下,基因表达发生的改变也是可以遗传的,导致可遗传的表现型变化。表观遗传学主要包括DNA甲基化作用、组蛋白修饰作用、染色质重塑、遗传印记、随机染色体(X)失活及RNA世界等。与表观遗传学相关的疾病主要有肿瘤、心血管病、精神病和自身免疫系统性病等。现就表观遗传学与疾病进行综述。     

Is it a revolution?

Jablonka and Lamb's claim that evolutionary biology is undergoing a ‘revolution’ is queried. But the very concept of revolutionary change has uncertain application to a field organized in the manner of contemporary biology. The explanatory primacy of sequence properties is also discussed.

An integrated strategy for identification of both sharp and broad peaks from next-generation sequencing data

A novel integrative approach has been developed by Lieb and colleagues for analyzing genome-wide datasets of different chromatin-binding factors and epigenetic states that exhibit both sharp and diffuse signals on the genome.     

Conversion of Mouse Epiblast Stem Cells to an Earlier Pluripotency State by Small Molecules

Epiblast stem cells (EpiSCs) are pluripotent cells derived from post-implantation late epiblasts in vitro. EpiSCs are incapable of contributing to chimerism, indicating that EpiSCs are less pluripotent and represent a later developmental pluripotency state compared with inner cell mass stage murine embryonic stem cells (mESCs). Using a chemical approach, we found that blockage of the TGFβ pathway or inhibition of histone demethylase LSD1 with small molecule inhibitors induced dramatic morphological changes in EpiSCs toward mESC phenotypes with simultaneous activation of inner cell mass-specific gene expression. However, full conversion of EpiSCs to the mESC-like state with chimerism competence could be readily generated only with the combination of LSD1, ALK5, MEK, FGFR, and GSK3 inhibitors. Our results demonstrate that appropriate synergy of epigenetic and signaling modulations could convert cells at the later developmental pluripotency state to the earlier mESC-like pluripotency state, providing new insights into pluripotency regulation.     

The CpG island methylator phenotype in colorectal cancer: Progress and problems

In recent years, attention has focused on the biology and potential clinical importance of the CpG island methylator phenotype (CIMP) in colorectal cancer (CRC). While it is generally well accepted that etiologically and clinically distinct subgroups exist in this disease, a precise definition of CIMP remains to be established. Here, we summarize existing literature that documents the prevalence of CIMP in CRC, with particular attention to the various methods and definitions used to classify a tumor as CIMP positive. Through a systematic review on both case-series and population based studies, we examined only original research articles reporting on sporadic CRC and/or adenomas in unselected cases. Forty-eight papers published between January 1999 and August 2011 met the inclusion criteria. We describe the use of multiple gene panels, marker threshold values, and laboratory techniques which results in a wide range in the prevalence of CIMP. Because there is no universal standard or consensus on quantifying the phenotype, establishing its true prevalence is a challenge. This bottleneck is becoming increasingly evident as molecular pathological epidemiology continues to offer possibilities for clear answers regarding environmental risk factors and disease trends. For the first time, large, unselected series of cases are available for analysis, but comparing populations and pooling data will remain a challenge unless a universal definition of CIMP and a consensus on analysis can be reached, and the primary cause of CIMP identified.